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october exam > pharm 2 > Flashcards

pharm 2 Flashcards

1
Q

moa of propofol

A

direct gaba a agonist-> increased cl conductance-> neuronal hyperpolarization

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2
Q

doa of propofol

A

5-10 mins

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3
Q

clearance of propofol

A

liver (p450) and extrahepatic metabolism (lungs)

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4
Q

which way does co2 response curve get shifted with propofol

A

down and to R (less sensitive to co2)

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5
Q

what does propofol do to hypoxic ventilatory drive

A

inhibits it

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6
Q

does propofol effect myocardial contractility

A

decreases it

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7
Q

does propofol effect venous tone

A

yes- decreased preload

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8
Q

cns effects of propofol

A

no analgesia!

dec cbf, icp, iop, cmro2

anticonvulsant properties

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9
Q

what is propofol made of

A

egg lecithin, soybean oil, glycerol

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10
Q

what allergy is a concern with propofol

A

egg allergy is fine - egg lecithin comes from the yolk- most egg allergy is to albumin in egg white

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11
Q

propofol infusion syndrome risk factors

A

-propofol dose > 4 mg/kg/hr
-propofol infusion duration >48 hrs
-adults > children
-inadequate oxygen delivery
-sepsis
-significant cerebral injury

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12
Q

clinical presentation of propofol infusion syndrome

A

-acute refractory bradycardia -> asystole

+
-metabolic acidosis
-rhabdo
-enlarged/ fatty liver
-renal failure
-HLD
-lipemia (cloudy plasma or blood)

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13
Q

how long is a propofol syrnige good for

A

6 hrs

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14
Q

how long is prop infusion good for

A

12 hrs

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15
Q

what preservatives are in propofol

A

diprivan contains edta

generic propofol- different preservatives- metabisulfite - bronchospasm; benzyl alcohol in infants

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16
Q

propofol injection pain can be minimized/ eliminated by

A

-injecting into lg more proximal vein
-lidocaine (before or mixed)
-opioid before propofol

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17
Q

what amount of propofol is used for ponv

A

10-20 mg IV

infusion: 10 mcg/kg/min

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18
Q

fospropofol

A

prodrug, propofol is active metabolite

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19
Q

what converts fospropofol to propofol

A

alkaline phosphatase

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20
Q

how does ketamine work

A

nmda antagonist (antagonizes glutamate)

seconday receptor targets opioid, MAO, serotonin, NE, muscarinic, na channels

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21
Q

what does ketamine dissociate

A

thalmus (sensory) from limbic system (awareness)

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22
Q

induction dose for ketamine

A

1-2 mg/kg

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23
Q

im ketamine dose

A

4-8 mg/kg

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24
Q

ketamine onset

A

iv 30-60 sec
im 2-4 min

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25
Q

duration of ketamine

A

10-20 min (may require 60-90 min for full orientation)

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26
Q

clearance for keramine

A

liver (p450 enzymes)

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27
Q

does ketamine make matabolizes

A

yes active metabolite: norketamine (1/3-1/5 potency of ketamine)

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28
Q

what does chronic ketamine use do

A

induces liver enzymes (burn patients)

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29
Q

when would increased SNS from ketamine be harmful

A

severe CAD

usually subhypnotic doses < 0.5 mg/kg usually doesnt activate SNS

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30
Q

myocardial effects of ketamine

A

myocardial depressant!!

it only increases CO, HR< SVR< PVR if you have intact SNS - depressant effects unmasked if pt has depleted catecholamine (sepsis) or sympathectomy

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31
Q

what pt do you need to be careful about the pvr effects of ketamine with

A

severe rv failure- causes increased pvr

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32
Q

respiratory effects of ketamine

A

-bronchodilation (great choice if pt is actively wheezing)
-upper airway muscle tone and airway reflexes remain intact
-does not significantly shift co2 response curve
-increased oral and pulmonary secretions- increased risk of laryngospasm

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33
Q

cns effects

A

increased cmro2, cbf, icp, eeg, nystagmus, emergence delirium

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34
Q

emergence delirium what is it and how to prevent

A

-presents as nightmares and hallucinations (risk for up to 24 hours)
-benzos are most effective way to prevent emergent delirium (versed > diazepam)

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35
Q

risks for emergence delirium

A

age > 15 yrs, female, ketamine > 2 mg/kg, hx of personality disorder

36
Q

ketamine analgesia properties

A

-good analgesia and opioid sparing effect (only induction agent that does this)
-somatic pain > visceral pain
-blocks central sensitization and wind up in dorsal horn of spinal cord
-prevents opioid induced hyperalgesia (after remifentinal infusion)
-excellent for burn patients and those with pre existing chronic pain syndromes

37
Q

duration of etomidate

A

5-15 min

38
Q

etomidate clearance

A

hepatic p450 enzymes and plasma esterases

39
Q

cv effects

A

-minimal change in HR, SV or CO
-SVR decreased- small reduction in bp
-does not block sns response to laryngoscopy- give esmolol or opioid

mild resp depression (less than versed or prop)

40
Q

cns effects

A

dec: cmro2, cbf, icp
cpp remains stable
no analgesia

41
Q

muscle side effect with etomidate

A

myoclonus- involuntary skeletal muscle contraction, dystonia or tremor

likely due to imbalance between excitatory and inhibatory pathways of thalamocortical tract

NOT a seizure

42
Q

relationship between etomidate and seizures

A

no hx of seizures- no increased risk

hx of seizures- can increase seizure like activity and possibly increase seizure risk

43
Q

adrenocortical suppression and etomidate

A

cortisol and aldosterone synthesis are dependent on enzyme 11 beta hydrozylase (located in adrenal medulla)

etomidate inhibits 11 beta hydrozylase and 17 alpha hydroxylase

44
Q

how long does adrenocortical function suppression last with etomidate

A

5-8 hours (some say up to 24)

no etomidate in sepsis pt!

45
Q

2 subclasses of barbituates

A

thiobarbituates- sulfur molecule in 2nd position

oxybarbituate- oxygen molecule in 2nd position

46
Q

GABA a agonist

A

depresses reticular activating system in brainstem

low/normal dose: increases affinity of gaba

high dose: directly stimulates gaba a

47
Q

onset and duration of thiopental

A

onset: 30-60 seconds

duration: 5-10 mins

48
Q

clearance of thiopental

A

liver (p450 enzymes)

redistribution (not metabolism) determines awakening

49
Q

what happens with repeated doses of thiopental

A

tissue accumulation-> prolonged wake up time-> hangover effect

50
Q

cv effects of thiopental

A

-hypotension (venodiilation, dec preload, myocardial depression)
-non immunogenic histamine release
-baroreceptor preserrved- reflex tachycardia

51
Q

resp effects of thiopental

A

-co2 curve shifted right (resp depression)
-histamine-> bronchocontriction (caution if asthma!!)

52
Q

cns effects of thiopental

A

decreased cmro2, cbf, icp, eeg

53
Q

does thiopental have analgesia

A

no- low dose may increase perception of pain

54
Q

acute intermittent porphyria

A

a defect in heme synthesis- promotes accumulation of heme precurosors (ALA induction)

this type is most common and dangerous type

55
Q

what drugs do you avoid with acute intermittent prophoryia

A

any drugs that induce ALA synthase

barbs, etomidate, ketamine, toradol, amiodarone, ccb, birth control

56
Q

tx for acute intermittent porphorya

A

-liberal hydration, glucose supplementation (reduces ALA synthase activity), heme arginagte, prevention of hypothermia

57
Q

what happens if you inject thiopental intra arterial

A

tissue necrosis

tx: phentolamine or phenoxybenzamine

58
Q

gold standard for induction during ect

A

methohexital

decreases seizure threshold- better quality seizure

59
Q

induction dose of methohexital

A

1-1.5 mg/kg

60
Q

MOA of precedex

A

alpha 2 agonist-> decreases camp-> inhibits locus coerulus in pons (sedation)

61
Q

how does analgesia get produced by precedex

A

alpha 2 stim in dorsal horn of spinal cord (decreases glutamate and substance P release)

62
Q

dose of precedex

A

loading: 1 mcg/kg over 10 min

maintence: 0.4-0.7 mcg/kg/hr

63
Q

onset and duration of precedex

A

onset 10-20 min
duration 10-30 min (after d/c infusion)

64
Q

clearance of precedex

A

liver (p450)

65
Q

most common side effects of precedex

A

brady and hotn

66
Q

rapid admin of precedex can cause

A

htn (alpha 2 stim)

usually short lived

67
Q

cns eeffects of dex

A

produces sedation resembling natural sleep (unique in this)

-no reliable amnesia
-pt arouses easily

-dec cbf
-no change in cmro2
-no change in icp

68
Q

chemical make up of midazolam- how does this affect solubility

A

imidazole ring

acidic ph- ring opens- increasing water solubility

physiologic ph- ring closes- increasing lipid solubility

69
Q

is midazolam water or lipid soluble in the vial

A

water

needs no solvent like propylene glycol (diazepam and lorazepam need this)

70
Q

MOA or midazolam

A

gaba a agonist- increases frequency of channel opening-> neuronal hyperpolarization

most gaba a agonists increase channel open time but benzos increase open frequency

71
Q

po dose in children for versed

A

0.5- 1 mg/kg

72
Q

what is po bioavaliability of midazolam

A

po bioavaliability is 50% due to significant first pass metabolism

73
Q

iv induction of versed dose

A

0.1-0.4 mg/kg

74
Q

what induction agents produce an active metabolite

A

ketamine, versed, fospropofol

75
Q

what agents have no active metabolites

A

precedex, propofol, etomidate

76
Q

cv effects of versed (sedation vs induction)

A

sedation: minimal
induction: dec svr and bp

77
Q

cns effects of versed

A

sedation: minimal effects of cmro2 and cbf

induction: decreases both

78
Q

what agents can produce isoelectric eeg

A

propofol and barbs (versed cannot!)

79
Q

does versed do analgesia

A

no

80
Q

remimazolam

A

-ultra short acting benzo
-vial needs to be protected from light
-discard single use vial after 8 hrs

81
Q

who is remimidazolam c/i in

A

pt with severe hypersensitivity rxn to dextran 40

82
Q

benzo reversal

A

flumazenil (high affinity)

83
Q

doa of flumazenil

A

30-60 min

84
Q

dosing of flumazenil

A

0.2 mg IV (titrated in 0.1 mg increments q1 min)

85
Q

potential side effects of flumazenil

A

does not increase sns tone, anxiety or neuroendocrine evidene of stress (narcan does!)

but it can show signs of withdrawl including seizures

86
Q
A

october exam (12 decks)

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